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. Author manuscript; available in PMC: 2009 Aug 15.
Published in final edited form as: Cancer Res. 2008 Aug 15;68(16):6643–6651. doi: 10.1158/0008-5472.CAN-08-0850

Figure 2. Inhibition of GSK3 activity in glioma cell lines leads to changes in glucose regulation and in anti-apoptotic mechanisms in mitochondria.

Figure 2

(A) Western Blot analysis of GSK3 siRNAs treated cell lysates show that GSK3 siRNAs decrease S640 phosphorylation of GYS in U251 (48 hours after transfection). (B) Bar graph shows glucose levels decrease in U251 cells treated with enzastaurin, 5 μM for 4 hours. Immunocytochemistry staining with anti-glycogen antibody revealed that GSK3 inhibition resulted in increased glycogen stores in the glioma cells. U251 cells were treated with (a) DMSO (4hours), (b) enzastaurin, 5μM (4hours); (c) insulin (30 minutes); (d) glucoamylase (3 hours) Glucoamylase digests glycogen and therefore is used as a negative control. The similar data were obtained with 705701 and LY2064827. (C) Western blot analysis of Bax levels in U251 treated with control or GSK3 siRNA. (D) Ratio of Bax/HK activity in mitochondria fractions is increased with GSK3 siRNA (48 hours) and enzastaurin treatments (4 hours). MitoTracker® Green staining of the functional mitochondria in DMSO and 5μM enzastaurin treated living U251 cells. Red color in the right panel shows fluorescence of enzastaurin.

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